Exploring the groundbreaking hypothesis linking smoking to Hidradenitis Suppurativa and its implications for treatment and prevention.
For the millions living with Hidradenitis Suppurativa (HS), the condition is a source of chronic pain and social isolation. This inflammatory skin disease, characterized by painful, boil-like lumps in skin folds, has long puzzled physicians. But what if a key to understanding this debilitating condition has been hiding in plain sight? Enter the provocative concept of "smoker's boils"—a theory that directly links tobacco smoking to HS and is reshaping how dermatologists understand, diagnose, and treat this stubborn condition.
Research indicates that up to 90% of HS patients are smokers, a statistic that demands explanation. This article explores the groundbreaking hypothesis that reframes HS as "smoker's boils," examining the compelling evidence behind this connection and what it means for the future of treatment.
of HS patients are smokers
more common in women
higher risk for smokers
Hidradenitis Suppurativa is a chronic inflammatory condition that goes far beyond typical skin problems. It manifests as painful, recurrent lumps that typically appear in areas where skin rubs together, such as the armpits, groin, buttocks, and under the breasts.
These lesions aren't ordinary boils—they represent a complex dysfunction of hair follicles that can lead to tunnels under the skin, persistent drainage of pus, and significant scarring.
The impact of HS extends well beyond physical symptoms. The condition can be embarrassing and isolating due to its location, drainage, and odor. Studies show that people with HS experience higher rates of anxiety and depression than the general population 1 .
Until recently, the understanding of HS has been fragmented. The condition was once mistakenly thought to be primarily an infection of sweat glands, leading to the inappropriate name "acne inversa." We now know that HS begins with blockage of hair follicles, but what causes this initial blockage remains the central mystery.
Traditional risk factors identified include:
While these factors provide some insight, they haven't yielded consistently effective treatments for all patients.
In 2011, researchers Rudolf Happle and Arne König proposed a revolutionary idea: that HS lesions in smokers represent a distinct entity that should be called "smoker's boils" 2 . This wasn't merely a change in terminology but a fundamental reconceptualization of the condition's origin.
The proposal emerged from simple clinical observation—the overwhelming majority of their HS patients were regular tobacco users. This pattern was too consistent to dismiss as coincidence. They argued that recognizing this connection could enable earlier diagnosis and more targeted prevention, particularly through smoking cessation.
"If patients stop smoking at such an early stage of HS, they most likely have a chance that this devastating disease will not progress."
The implications are profound. If smoking is indeed a primary trigger rather than just an associated factor, it transforms HS from an unavoidable genetic fate to a potentially preventable condition for many patients. The hypothesis also provides a testable framework for researching the biological mechanisms behind HS development.
From "unavoidable genetic condition" to "potentially preventable smoking-related disease"
Happle and König propose "smoker's boils" hypothesis
Landmark population study confirms smoking-HS link
Comprehensive review of biological mechanisms
Dose-response relationship established
While early observations were compelling, the smoker's boils hypothesis required validation through large-scale population studies. This evidence arrived in 2018 with a groundbreaking study published in the British Journal of Dermatology that examined the relationship between smoking and HS incidence at a population level 3 .
The research team, led by Dr. Amit Garg, conducted a retrospective cohort analysis of health data from the United States. Their approach was both comprehensive and meticulous:
The findings provided the strongest evidence to date linking smoking to HS:
HS incidence among smokers
HS incidence among non-smokers
This translates to smokers facing twice the risk of developing HS compared to non-smokers.
As senior author Dr. Amit Garg noted, "This is the first population level evidence that tobacco smoking is a true risk factor for the development of Hidradenitis suppurativa." 3
| Subgroup | HS Incidence | Risk Comparison |
|---|---|---|
| Overall smoker population | 0.20% | 1.8x higher than non-smokers |
| Non-smokers | 0.11% | Reference group |
| Smokers aged 30-39 | 0.35% | Particularly high-risk age group |
| Female smokers | 0.28% | Higher than male smokers |
| African American smokers | 0.46% | Highest incidence among racial groups |
| Obese smokers (BMI ≥30) | 0.33% | Combined effect of two risk factors |
Recent investigations have further refined our understanding of the smoking-HS relationship. A 2025 study published in PLoS One examined how changes in smoking intensity affect HS risk, particularly in people with Type 2 diabetes—another HS risk factor 4 .
This research analyzed data from 1.7 million participants in the Korean National Health Insurance Service. The findings revealed a dose-response relationship: individuals who increased their cigarette consumption had a 28.5% higher HS risk compared to nonsmokers, while those who continued smoking at stable levels had a 23.6% increased risk.
| Smoking Behavior | Increased HS Risk | Clinical Implications |
|---|---|---|
| Never smokers | Reference group | Baseline risk |
| Sustained smokers | 23.6% higher risk | Continuous smoking maintains elevated risk |
| Increased smoking intensity | 28.5% higher risk | Dose-response relationship evident |
| Smoking cessation | Risk reduction likely | Emerging evidence supports benefit |
While the exact mechanisms remain under investigation, several theories have emerged about how smoking might trigger or worsen HS:
Tobacco components may alter the skin microbiome or directly irritate hair follicles, leading to blockage and inflammation
Nicotine and other chemicals may disrupt normal immune responses, creating chronic inflammation in susceptible individuals
Smoking might increase the virulence of skin bacteria or weaken natural defenses against infection
As noted in a comprehensive 2020 review, the relationship between smoking and HS involves a complex interplay of environmental, genetic, and immunological factors that researchers are still working to unravel 5 .
Understanding the smoking-HS connection requires sophisticated research approaches. Scientists in this field employ several key methods and tools:
| Research Tool | Primary Function | Application in HS-Smoking Research |
|---|---|---|
| Retrospective cohort design | Analyze existing health data | Identify patterns in large populations over time |
| Electronic health records | Provide real-world clinical data | Study HS incidence across diverse demographics |
| Smoking status questionnaires | Standardize smoking exposure data | Categorize patients by smoking intensity and history |
| HS diagnostic criteria (ICD-10 code L73.2) | Ensure consistent HS identification | Enable accurate case identification in databases |
| Multivariate statistical analysis | Control for confounding variables | Isolate smoking effect from obesity, age, genetics |
| Incidence rate calculation | Measure new disease cases | Compare HS development in smokers vs. non-smokers |
The recognition of HS as "smoker's boils" has transformed clinical practice and patient education. Dermatologists now emphasize smoking cessation as a cornerstone of HS management.
Studies indicate that smokers with HS have lower treatment response rates—only 29% of smokers achieved remission compared to 40% of nonsmokers in one study 6 .
The concept of "smoker's boils" represents more than just a name change—it signifies a fundamental shift in how we understand and approach a debilitating condition. By recognizing the central role of smoking in HS pathogenesis, researchers have opened new avenues for prevention, early detection, and treatment.
For the millions affected by HS, this new paradigm offers tangible hope. While not all HS cases are smoking-related (approximately 10% occur in nonsmokers), the evidence suggests that for the majority of patients, smoking cessation could significantly alter the disease course.
The message is clear: quitting smoking provides not only general health benefits but also a powerful specific intervention for managing HS.
As research continues to unravel the complex relationship between tobacco and this painful skin condition, the concept of "smoker's boils" stands as a powerful example of how clinical observation, population research, and testable hypotheses can combine to advance medical understanding and improve patient care.
Clinical pattern recognition
Testable framework development
Population-level evidence
Clinical practice transformation